Physiological Glossary

Key terms and definitions for NCLEX Physiological Integrity.

Physiological Integrity - Key Nursing Terms

Arterial Blood Gases (ABGs)
A diagnostic test measuring the pH, partial pressure of oxygen (PaO2), partial pressure of carbon dioxide (PaCO2), bicarbonate (HCO3-), and oxygen saturation (SaO2) in arterial blood. Normal values: pH 7.35-7.45, PaCO2 35-45 mmHg, HCO3- 22-26 mEq/L, PaO2 80-100 mmHg. Used to assess acid-base balance and oxygenation status.
Respiratory Acidosis
An acid-base imbalance caused by CO2 retention due to hypoventilation. ABG findings: pH <7.35, PaCO2 >45 mmHg. Causes include COPD, respiratory depression from opioids, pneumonia, and airway obstruction. Treatment focuses on improving ventilation: bronchodilators, oxygen therapy, mechanical ventilation, and reversing the underlying cause.
Respiratory Alkalosis
An acid-base imbalance caused by excessive CO2 elimination due to hyperventilation. ABG findings: pH >7.45, PaCO2 <35 mmHg. Causes include anxiety, pain, fever, hypoxia, and mechanical overventilation. Treatment includes addressing the underlying cause; rebreathing into a paper bag may be used for anxiety-induced hyperventilation.
Metabolic Acidosis
An acid-base imbalance caused by accumulation of acid or loss of bicarbonate. ABG findings: pH <7.35, HCO3- <22 mEq/L. Causes include diabetic ketoacidosis, renal failure, lactic acidosis, severe diarrhea, and salicylate toxicity. Kussmaul respirations (deep, rapid breathing) represent respiratory compensation. Treatment addresses the underlying cause; sodium bicarbonate may be given in severe cases.
Metabolic Alkalosis
An acid-base imbalance caused by loss of acid or excess bicarbonate retention. ABG findings: pH >7.45, HCO3- >26 mEq/L. Causes include prolonged vomiting or nasogastric suctioning, excessive antacid use, and hypokalemia. Respiratory compensation involves shallow, slow breathing. Treatment includes fluid and electrolyte replacement, particularly potassium and chloride.
Compensation
The body's physiological response to an acid-base imbalance in which the system not primarily affected (respiratory or renal) attempts to restore normal pH. Respiratory compensation occurs within minutes to hours by adjusting CO2 levels through changes in ventilation rate and depth. Renal compensation occurs over hours to days by adjusting bicarbonate reabsorption and hydrogen ion excretion.
Hypokalemia
Serum potassium level below 3.5 mEq/L. Causes include diuretic therapy, vomiting, diarrhea, and inadequate intake. Manifestations include muscle weakness, leg cramps, decreased bowel motility (ileus), shallow respirations, cardiac dysrhythmias (flattened T waves, U waves, ST depression), and increased digoxin toxicity risk. IV potassium must always be diluted and administered via infusion pump; never given as IV push.
Hyperkalemia
Serum potassium level above 5.0 mEq/L. Causes include renal failure, potassium-sparing diuretics, ACE inhibitors, tissue destruction, and metabolic acidosis. Manifestations include muscle weakness, paresthesias, bradycardia, tall peaked T waves, widened QRS, and risk of cardiac arrest. Emergency treatment includes IV calcium gluconate, insulin with dextrose, sodium bicarbonate, and kayexalate.
Hyponatremia
Serum sodium level below 136 mEq/L. Causes include SIADH, excessive water intake, diuretic use, and adrenal insufficiency. Manifestations include nausea, headache, confusion, lethargy, seizures, and cerebral edema. Severe cases may require hypertonic saline (3% NaCl) administered slowly with frequent monitoring to prevent osmotic demyelination syndrome (central pontine myelinolysis).
Hypernatremia
Serum sodium level above 145 mEq/L. Causes include dehydration, diabetes insipidus, excessive sodium intake, and Cushing syndrome. Manifestations include extreme thirst, dry mucous membranes, restlessness, agitation, seizures, and altered level of consciousness. Treatment involves gradual replacement of water deficit using hypotonic solutions (0.45% NaCl) to prevent cerebral edema.
Hypocalcemia
Serum calcium level below 9.0 mg/dL (total) or ionized calcium below 4.5 mg/dL. Causes include hypoparathyroidism, vitamin D deficiency, chronic kidney disease, and blood transfusions (citrate binding). Manifestations include numbness and tingling, Trousseau sign (carpal spasm with BP cuff inflation), Chvostek sign (facial twitching with tapping), hyperactive reflexes, tetany, and seizures.
Hypercalcemia
Serum calcium level above 10.5 mg/dL. Causes include hyperparathyroidism, malignancy, prolonged immobility, and excessive vitamin D or calcium intake. Manifestations include muscle weakness, decreased deep tendon reflexes, constipation, polyuria, kidney stones, shortened QT interval, confusion, and lethargy. Treatment includes IV normal saline for hydration, loop diuretics, calcitonin, and bisphosphonates.
Intravenous (IV) Therapy
The administration of fluids, medications, blood products, or nutrients directly into a vein. Types of IV solutions include isotonic (0.9% NaCl, lactated Ringer's), hypotonic (0.45% NaCl), and hypertonic (3% NaCl, D10W). Isotonic solutions expand intravascular volume without shifting fluid between compartments. Hypotonic solutions shift fluid into cells. Hypertonic solutions pull fluid from cells into the vascular space.
IV Complications
Adverse events associated with intravenous therapy. Infiltration (non-vesicant fluid leaking into surrounding tissue): cool, pale, swollen site. Extravasation (vesicant medication leaking): tissue damage and necrosis. Phlebitis (vein inflammation): redness, warmth, pain along the vein. Air embolism: dyspnea, chest pain; position patient in left Trendelenburg. Central line-associated bloodstream infection (CLABSI): prevented through bundle practices.
Blood Transfusion
The administration of blood components. Requires verification by two licensed nurses of patient identification, blood type, Rh factor, crossmatch compatibility, expiration date, and unit number. Infuse within 4 hours. Monitor for transfusion reactions: acute hemolytic (fever, flank pain, hemoglobinuria), febrile non-hemolytic, allergic (urticaria, pruritus), and anaphylaxis. Stop transfusion immediately for any reaction, maintain IV access with normal saline.
Pharmacokinetics
The study of drug movement through the body, comprising four processes: absorption (drug entry into the bloodstream), distribution (transport to target tissues), metabolism (biotransformation, primarily in the liver via cytochrome P450 enzymes), and excretion (elimination, primarily via the kidneys). These processes determine onset, peak, duration, and therapeutic drug levels.
Half-Life
The time required for the plasma concentration of a drug to decrease by 50%. Determines dosing frequency; drugs with short half-lives require more frequent dosing. Steady-state concentration is generally achieved after approximately 4-5 half-lives of consistent dosing. Factors affecting half-life include hepatic and renal function, age, and drug interactions.
Therapeutic Drug Monitoring
The measurement of drug concentrations in blood to optimize efficacy and minimize toxicity. Trough levels (drawn just before the next dose) assess minimum concentration. Peak levels (drawn after distribution) assess maximum concentration. Commonly monitored drugs include vancomycin (trough 10-20 mcg/mL), gentamicin (peak 5-10 mcg/mL, trough <2 mcg/mL), lithium, digoxin, phenytoin, and theophylline.
Cardiac Output
The volume of blood pumped by the heart per minute, calculated as heart rate multiplied by stroke volume. Normal cardiac output is approximately 4-8 L/min. Cardiac index adjusts for body surface area (normal 2.5-4.0 L/min/m2). Affected by preload, afterload, contractility, and heart rate. Decreased cardiac output manifests as hypotension, tachycardia, decreased urine output, cool extremities, and altered mental status.
Preload
The volume of blood in the ventricles at the end of diastole (end-diastolic volume), representing the degree of myocardial fiber stretch before contraction. Increased by IV fluids and blood transfusions. Decreased by diuretics, vasodilators (nitroglycerin), and hemorrhage. Central venous pressure (CVP) and pulmonary artery wedge pressure (PAWP) are clinical measures of right and left heart preload, respectively.
Afterload
The resistance the ventricles must overcome to eject blood during systole. Primarily determined by systemic vascular resistance (SVR) for the left ventricle and pulmonary vascular resistance (PVR) for the right ventricle. Increased afterload (vasoconstriction) increases cardiac workload. Reduced by vasodilators (ACE inhibitors, nitroprusside) and intra-aortic balloon pump counterpulsation.
Shock
A life-threatening condition of inadequate tissue perfusion resulting in cellular oxygen deprivation. Types include hypovolemic (fluid/blood loss), cardiogenic (pump failure), distributive (septic, anaphylactic, neurogenic), and obstructive (cardiac tamponade, tension pneumothorax, pulmonary embolism). General management: identify and treat the cause, ensure airway, provide fluid resuscitation (except cardiogenic), and administer vasopressors as needed.
Sepsis
A life-threatening organ dysfunction caused by a dysregulated host response to infection. Identified by acute change in SOFA score of 2 or more points. Septic shock adds vasopressor requirement to maintain MAP of 65 mmHg or greater and serum lactate greater than 2 mmol/L despite adequate volume resuscitation. Treatment follows the Surviving Sepsis Campaign guidelines: early antibiotics, fluid resuscitation (30 mL/kg crystalloid within 3 hours), blood cultures before antibiotics, and lactate-guided resuscitation.
Electrocardiogram (ECG/EKG)
A graphical recording of the electrical activity of the heart. Normal sinus rhythm: regular rate of 60-100 bpm, consistent P waves preceding each QRS complex, PR interval 0.12-0.20 seconds, QRS duration 0.06-0.12 seconds. Common abnormalities include atrial fibrillation (irregularly irregular, no P waves), ventricular tachycardia (wide QRS, rapid rate), and ventricular fibrillation (chaotic waveform, no identifiable complexes).
Troponin
A cardiac-specific protein released into the bloodstream when myocardial cells are damaged. Troponin I and troponin T are highly sensitive and specific biomarkers for myocardial infarction. Levels rise within 3-6 hours of injury, peak at 12-24 hours, and may remain elevated for 7-14 days. Serial measurements help confirm or rule out acute coronary syndrome.
Mechanical Ventilation
Life-support intervention that uses a machine to assist or replace spontaneous breathing. Key settings include tidal volume (6-8 mL/kg ideal body weight for lung-protective ventilation), respiratory rate, FiO2 (fraction of inspired oxygen), and PEEP (positive end-expiratory pressure, prevents alveolar collapse). Nursing care includes HOB elevation of 30-45 degrees, oral care every 2 hours, DVT prophylaxis, sedation vacation, and daily spontaneous breathing trials per the ventilator bundle to prevent VAP.
Chest Tube Management
Care of a closed drainage system used to remove air, blood, or fluid from the pleural space. The drainage system maintains a water seal to prevent air re-entry. Tidaling (fluctuation in the water seal chamber with respiration) indicates proper function. Continuous bubbling in the water seal suggests an air leak. The chest tube should never be clamped except briefly for system changes. Keep the drainage system below chest level at all times.
Glasgow Coma Scale (GCS)
A standardized neurological assessment tool measuring level of consciousness. Evaluates three responses: eye opening (1-4), verbal response (1-5), and motor response (1-6). Total score ranges from 3 (deep coma) to 15 (fully alert). A score of 8 or less generally indicates coma and the need for airway protection. Used for serial assessment to detect neurological deterioration.
Increased Intracranial Pressure (ICP)
Elevation of pressure within the cranial vault above the normal range of 5-15 mmHg. Causes include traumatic brain injury, hemorrhage, tumor, hydrocephalus, and cerebral edema. Early signs: headache, decreased level of consciousness, restlessness. Late signs: Cushing's triad (hypertension, bradycardia, irregular respirations), unilateral pupil dilation, posturing. Interventions include HOB elevation to 30 degrees, maintaining head midline, avoiding Valsalva maneuver, osmotic diuretics (mannitol), and hyperventilation in acute herniation.
Digoxin
A cardiac glycoside used to treat heart failure and atrial fibrillation. Increases myocardial contractility (positive inotrope) and decreases heart rate (negative chronotrope). Therapeutic serum level: 0.8-2.0 ng/mL. Always assess apical pulse for one full minute before administration; hold if pulse is below 60 bpm in adults. Signs of toxicity include nausea, vomiting, visual disturbances (yellow-green halos), and dysrhythmias. Hypokalemia increases toxicity risk.
Heparin
An anticoagulant that inhibits thrombin and factor Xa, preventing clot formation. Administered IV (continuous drip) or subcutaneously. Monitored by activated partial thromboplastin time (aPTT); therapeutic goal is typically 1.5-2.5 times the control value. Antidote is protamine sulfate. Adverse effects include bleeding and heparin-induced thrombocytopenia (HIT). Platelet counts are monitored regularly.
Warfarin
An oral anticoagulant that inhibits vitamin K-dependent clotting factors (II, VII, IX, X). Monitored by prothrombin time (PT) and International Normalized Ratio (INR); therapeutic INR is typically 2.0-3.0 (2.5-3.5 for mechanical heart valves). Antidote is vitamin K (phytonadione). Numerous drug and food interactions exist; patients should maintain consistent vitamin K intake. Teratogenic; contraindicated in pregnancy.
Diabetes Mellitus
A group of metabolic diseases characterized by hyperglycemia. Type 1: autoimmune destruction of pancreatic beta cells, requiring exogenous insulin. Type 2: insulin resistance with progressive insulin secretory defect, managed with lifestyle modifications, oral hypoglycemics, and/or insulin. Monitoring includes fasting blood glucose (normal 70-100 mg/dL) and HbA1c (goal <7% for most adults). Complications include hypoglycemia, DKA (type 1), HHS (type 2), neuropathy, retinopathy, and nephropathy.
Hypoglycemia
Blood glucose level below 70 mg/dL. Manifestations include tremors, diaphoresis, tachycardia, pallor, hunger, confusion, irritability, and seizures. Conscious patients: administer 15-20 grams of fast-acting carbohydrate (4 oz juice, glucose tablets), recheck in 15 minutes, repeat if still below 70 mg/dL (Rule of 15). Unconscious patients: administer IV dextrose 50% or IM glucagon.
Diabetic Ketoacidosis (DKA)
A life-threatening complication of diabetes (primarily type 1) characterized by hyperglycemia (usually >300 mg/dL), ketonemia, metabolic acidosis (pH <7.30, HCO3- <18 mEq/L), and dehydration. Presents with Kussmaul respirations, fruity breath odor, nausea, vomiting, and abdominal pain. Treatment includes IV fluid resuscitation with normal saline, continuous insulin infusion, electrolyte replacement (especially potassium), and monitoring for cerebral edema.
Complete Blood Count (CBC)
A laboratory test measuring components of blood. Key values: WBC 5,000-10,000/mm3 (infection, leukemia if elevated; immunosuppression if decreased), RBC 4.2-6.1 million/mm3, hemoglobin 12-18 g/dL, hematocrit 37-52%, platelets 150,000-400,000/mm3 (bleeding risk if <50,000; spontaneous bleeding if <20,000). Differential WBC identifies specific types of white blood cells.
Basic Metabolic Panel (BMP)
A blood test measuring key electrolytes and metabolic markers. Includes sodium (136-145 mEq/L), potassium (3.5-5.0 mEq/L), chloride (98-106 mEq/L), CO2/bicarbonate (22-26 mEq/L), BUN (10-20 mg/dL), creatinine (0.7-1.3 mg/dL), glucose (70-100 mg/dL fasting), and calcium (9.0-10.5 mg/dL). Elevated BUN and creatinine indicate impaired renal function; the BUN-to-creatinine ratio helps differentiate prerenal from intrinsic renal causes.